Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis
碩士 === 國立中興大學 === 生命科學系所 === 104 === Antizyme inhibitor (AZI) has been thought to promote cancer cell proliferation, it’s caused between with antizyme (AZ) and ornithine decarboxylase (Ornithine decarboxylase, ODC; EC 4.1.1.17) regulatory mechanism. Flavonoids source from fruits, vegetables, tea, wi...
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ndltd-TW-104NCHU51051112017-01-07T04:08:52Z http://ndltd.ncl.edu.tw/handle/76090874278192234590 Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis 類黃酮藉由抗酶抑制子調節機制參與HL-60自噬/分化/活化/凋亡 Yu-Teng Chang 張譽騰 碩士 國立中興大學 生命科學系所 104 Antizyme inhibitor (AZI) has been thought to promote cancer cell proliferation, it’s caused between with antizyme (AZ) and ornithine decarboxylase (Ornithine decarboxylase, ODC; EC 4.1.1.17) regulatory mechanism. Flavonoids source from fruits, vegetables, tea, wine, seeds or roots of plants, widely considered to have antioxidant or anti-inflammatory response effect. In our study, we chose four kinds of flavonoids: Epigallocatechin gallate (EGCG)、 Baicalein、 Myricetin、 7,8-Dihydroxyflavone (7,8-DHF), explore its toxic effect in HL-60 immunity cancer cell, and hoped that in the future can be further developed into new drugs for the treatment of leukemia or other cancers. Above these four drugs have been found to inhibit the ornithine decarboxylase enzyme activity, in our laboratory previous study have found catechin composition were impacted AZI protein structure, so we transfected AZI gene into HL-60, then compare whether those flavonoids affect AZI structure and function further impact toxic effect in cells. Moreover, many researches revealed TPA besides caused HL-60 differentiate to macrophage and induced autophagy, activation, differentiation and apoptosis. Based on these study we treat both EGCG and TPA in HL-60 and compare with empty vector and overexpression of AZI. Our data demonstrate those four drugs both could cause HL-60 apoptosis, but EGCG and myricetin caused overexpression of AZI more cell death than empty vector. Co-treated with TPA and EGCG compare with TPA only increase autophagy, activation, differentiation and apoptosis, and overexpression of AZI more strengthened on autophagy, activation, differentiation and apoptosis in HL-60. These results proved that TPA can cause HL-60 differentiation, and after add EGCG accelerates differentiation to cell death ahead of time. Therefore, in the future treatment of human leukemia, by TPA can mix with EGCG as an adjunct to anti-cancer therapy as a guideline. Hui-Chih Hung 洪慧芝 2016 學位論文 ; thesis 87 en_US |
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碩士 === 國立中興大學 === 生命科學系所 === 104 === Antizyme inhibitor (AZI) has been thought to promote cancer cell proliferation, it’s caused between with antizyme (AZ) and ornithine decarboxylase (Ornithine decarboxylase, ODC; EC 4.1.1.17) regulatory mechanism. Flavonoids source from fruits, vegetables, tea, wine, seeds or roots of plants, widely considered to have antioxidant or anti-inflammatory response effect. In our study, we chose four kinds of flavonoids: Epigallocatechin gallate (EGCG)、 Baicalein、 Myricetin、 7,8-Dihydroxyflavone (7,8-DHF), explore its toxic effect in HL-60 immunity cancer cell, and hoped that in the future can be further developed into new drugs for the treatment of leukemia or other cancers. Above these four drugs have been found to inhibit the ornithine decarboxylase enzyme activity, in our laboratory previous study have found catechin composition were impacted AZI protein structure, so we transfected AZI gene into HL-60, then compare whether those flavonoids affect AZI structure and function further impact toxic effect in cells. Moreover, many researches revealed TPA besides caused HL-60 differentiate to macrophage and induced autophagy, activation, differentiation and apoptosis. Based on these study we treat both EGCG and TPA in HL-60 and compare with empty vector and overexpression of AZI. Our data demonstrate those four drugs both could cause HL-60 apoptosis, but EGCG and myricetin caused overexpression of AZI more cell death than empty vector. Co-treated with TPA and EGCG compare with TPA only increase autophagy, activation, differentiation and apoptosis, and overexpression of AZI more strengthened on autophagy, activation, differentiation and apoptosis in HL-60. These results proved that TPA can cause HL-60 differentiation, and after add EGCG accelerates differentiation to cell death ahead of time. Therefore, in the future treatment of human leukemia, by TPA can mix with EGCG as an adjunct to anti-cancer therapy as a guideline.
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author2 |
Hui-Chih Hung |
author_facet |
Hui-Chih Hung Yu-Teng Chang 張譽騰 |
author |
Yu-Teng Chang 張譽騰 |
spellingShingle |
Yu-Teng Chang 張譽騰 Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis |
author_sort |
Yu-Teng Chang |
title |
Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis |
title_short |
Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis |
title_full |
Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis |
title_fullStr |
Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis |
title_full_unstemmed |
Flavonoids Participate in the Regulatory Mechanisms of Antizyme Inhibitor in HL-60 Autophagy/ Differentiation/ Activation/ Apoptosis |
title_sort |
flavonoids participate in the regulatory mechanisms of antizyme inhibitor in hl-60 autophagy/ differentiation/ activation/ apoptosis |
publishDate |
2016 |
url |
http://ndltd.ncl.edu.tw/handle/76090874278192234590 |
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